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作 者:欧志穗[1] 赖逸贵[2] 刘友章[1] 罗仁[3] 宋雅芳[4]
机构地区:[1]广州中医药大学第一附属医院二内科,广州510405 [2]南方医科大学中医药学院,广州510515 [3]南方医科大学附属南方医院,广州510515 [4]广州中医药大学脾胃研究所,广州510405
出 处:《中药新药与临床药理》2011年第4期407-410,共4页Traditional Chinese Drug Research and Clinical Pharmacology
基 金:广东省自然科学基金课题(06024137)
摘 要:目的研究胃炎Ⅰ号对慢性萎缩性胃炎(CAG)大鼠胃黏膜MMP1和TIMP1 mRNA表达的影响,探讨胃炎Ⅰ号对CAG大鼠胃黏膜损伤的疗效作用机制。方法将SD大鼠随机分为正常对照组和造模组,参照文献制造CAG模型;造模成功后采用胃炎I号煎剂高中低剂量(2.16,1.08,0.54 g.kg-1)及维酶素(0.86 g.kg-1)治疗CAG模型大鼠,实时荧光定量PCR技术检测MMP1及TIMP1 mRNA表达。结果与正常对照组比较,CAG组大鼠胃黏膜MMP1 mRNA表达降低(P<0.05),TIMP1 mRNA表达无明显变化(P>0.05);各治疗组与模型组比较,中剂量胃炎I号组对CAG大鼠胃黏膜病变疗效最佳,可提高MMP1 mRNA表达(P<0.05)。结论 CAG大鼠胃黏膜MMP1 mRNA表达水平下降,TIMP1 mRNA的表达未见明显异常,可能是慢性萎缩性胃炎的病理机制之一;胃炎I号可提高胃黏膜组织的MMP1 mRNA表达,有助于胃黏膜组织的修复,则是其治疗慢性萎缩性胃炎的作用机制之一。objective To observe the effect of Weiyan Recipe Ⅰ on the mRNA expression of MMP1 and TIMP1 in rats with chronic atrophic gastritis (CAG), and to explore its therapeutic mechanism for CAG. Methods SD rats were divided into model group and normal group. CAG model was established according to the related literatures. Then the model rats were divided into Vitacoenzyme Tablets(0.86 g·kg-1) group , and high-, middle- and low- dosage Weiyan Recipe Ⅰ groups (at the dosage of 2.16, 1.08, 0.54 g·kg-1 respectively). We detected the mRNA expression of MMP1 and TIMP1 by real-time fluorescent quantization PCR. Results Compared to the normal group, the mRNA expression of MMP1 was decreased(P 〈 0.05) , and the changes of TIMPlmRNA expression were not ob vious in the model rats(P 〉 0.05). Compared to the model group, the curative effect of the middle-dosage Weiyan Recipe I group was the best, and middle-dosage Weiyan Recipe I raised the mRNA expression of MMP1 in the CAG model rats(P 〈 0.05). Conclusion The mRNA expression of MMP1 is decreased while the mRNA expression of TIMP1 remains unchanged in the CAG model rats, which may be one of mechanism is one of pathogenic mechanisms of CAG. Weiyan Recipe Ⅰ could raise the mRNA expression of MMP1 in the CAG model rats, and is helpful to the repair of gastric mucous membrane, which is one of its possible therapeutic mechanisms for CAG.
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